Tropisms, taxes and the reflex arc

Plants respond to directional stimuli by tropisms, mediated by indoleacetic acid (IAA), an auxin.

• Phototropism: IAA is produced at the shoot tip and diffuses down; unilateral light causes it to move to the shaded side. In shoots, IAA promotes cell elongation, so the shaded side grows faster and the shoot bends towards the light — positive phototropism.
• Gravitropism: in roots, IAA accumulates on the lower side and inhibits elongation there, so the upper side grows faster and the root bends downwards — positive gravitropism. The same molecule, opposite effect, because the tissues respond differently.

Simple animal responses: a taxis is a directional movement towards or away from a stimulus (woodlice move away from light — negative phototaxis). A kinesis is non-directional: the animal changes its rate of turning — in unfavourable, dry conditions a woodlouse turns more often and moves faster, so by chance it spends more time in damp, dark places.

The Pacinian corpuscle, rods and cones

Every receptor is specific to one type of stimulus and acts as a transducer, converting that stimulus into a nervous impulse.

Pacinian corpuscle (pressure, in the skin): a sensory neurone ending wrapped in concentric lamellae of connective tissue. Pressure deforms the lamellae, which deforms stretch-mediated sodium ion channels in the neurone membrane. They widen, Na⁺ diffuses in, and the membrane depolarises to produce a generator potential. If it reaches the threshold, an action potential is triggered.

Rods vs cones:

• Rods — a single type of pigment (rhodopsin), so they give only monochrome vision. Many rods converge onto one bipolar cell, so their individual sub-threshold generator potentials can add up (spatial summation) to reach the threshold. Result: high sensitivity in dim light, but low visual acuity, because the brain cannot distinguish which rod was stimulated.
• Cones — three types (red-, green- and blue-sensitive iodopsins) → colour vision. Each cone generally has its own bipolar cell, so there is no summation: they need high light intensity to fire, but two adjacent cones stimulate two separate neurones, giving high visual acuity.
• Rods dominate the periphery of the retina; cones are concentrated at the fovea.

From the medulla to the sinoatrial node

Cardiac muscle is myogenic — it contracts of its own accord, without nervous stimulation. The rhythm is set by the sinoatrial node (SAN) in the wall of the right atrium, the pacemaker. The wave of depolarisation spreads across both atria, is delayed at the atrioventricular node (AVN) so that the atria finish emptying, then travels down the bundle of His and the Purkyne fibres to the apex, so the ventricles contract from the bottom upwards.

The rate is modified by the medulla oblongata, in response to two kinds of receptor:

• Chemoreceptors (in the carotid bodies, aorta and medulla) detect a fall in blood pH caused by rising CO₂. The medulla sends more impulses along the sympathetic nerve to the SAN, releasing noradrenaline and increasing heart rate — so more CO₂ is delivered to the lungs and removed.
• Baroreceptors (in the aorta and carotid sinus) detect blood pressure. If pressure is too high, impulses travel along the parasympathetic nerve (the vagus), releasing acetylcholine and slowing the heart. If pressure is too low, sympathetic stimulation raises it.

This is negative feedback in action, and it is why exercise raises heart rate before you consciously do anything: rising CO₂ from respiring muscle lowers blood pH, chemoreceptors fire, and the medulla increases the rate via the sympathetic nervous system.

Why exercise speeds the heart

Resting potential and the action potential

Resting potential (about −70 mV): the sodium–potassium pump actively transports 3 Na⁺ out for every 2 K⁺ in, using ATP. The membrane is far more permeable to K⁺ than to Na⁺ (K⁺ leak channels are open, voltage-gated Na⁺ channels are shut), so K⁺ diffuses back out. The inside is therefore negative relative to the outside — the axon is polarised.

• Depolarisation: a stimulus opens some voltage-gated Na⁺ channels; Na⁺ enters. If the threshold (−55 mV) is reached, more Na⁺ channels open — positive feedback — and the potential rockets to about +40 mV.
• Repolarisation: Na⁺ channels close; voltage-gated K⁺ channels open; K⁺ diffuses out and the inside becomes negative again.
• Hyperpolarisation: K⁺ channels are slow to close, so too much K⁺ leaves and the potential briefly overshoots below −70 mV. The Na⁺/K⁺ pump restores the resting potential.
• Refractory period: during this recovery no new action potential can be generated. This makes impulses discrete (they do not merge), makes them travel in one direction only, and sets an upper limit on impulse frequency.

All-or-nothing: a stronger stimulus does not give a bigger action potential. It gives a higher frequency of identical action potentials (and stimulates more neurones). That is how intensity is encoded.

Your turn — conduction speed

Your turn — maximum impulse frequency

Why myelin makes it fast

The cholinergic synapse

Synapses transmit chemically, which is slower than an axon but far more versatile.

• The action potential arrives at the presynaptic knob and opens voltage-gated calcium ion channels. Ca²⁺ diffuses in.
• Ca²⁺ causes synaptic vesicles to fuse with the presynaptic membrane and release acetylcholine (ACh) by exocytosis.
• ACh diffuses across the cleft and binds to complementary receptor proteins on the postsynaptic membrane, opening Na⁺ channels. Na⁺ enters and depolarises the postsynaptic membrane (an EPSP); if the threshold is reached, a new action potential is generated.
• Acetylcholinesterase in the cleft hydrolyses ACh into choline and ethanoic acid, which are reabsorbed and re-formed into ACh using ATP. Without this, the postsynaptic neurone would fire continuously.

Why synapses matter:

• Unidirectionality — only the presynaptic knob has vesicles, and only the postsynaptic membrane has receptors.
• Summation — spatial (several presynaptic neurones together) or temporal (one neurone firing rapidly) allows sub-threshold stimuli to add up and trigger an impulse.
• Inhibition — inhibitory synapses open Cl⁻ and K⁺ channels, hyperpolarising the membrane so that the threshold is harder to reach.

Neuromuscular junction: similar, but it is always excitatory, acts only on a muscle fibre (an endpoint, not a relay), and has many more receptors. ACh binds and depolarises the sarcolemma, and the impulse travels down the T-tubules.

The trigger at the synapse

The sliding filament mechanism

A myofibril is made of repeating sarcomeres: thin actin filaments (with tropomyosin and troponin wrapped around them) and thick myosin filaments with globular heads.

• Depolarisation of the sarcolemma spreads down the T-tubules to the sarcoplasmic reticulum, which releases Ca²⁺ into the sarcoplasm.
• Ca²⁺ binds to troponin, changing its shape and pulling tropomyosin aside to expose the myosin-binding sites on actin.
• Myosin heads bind to actin, forming cross-bridges. The head then bends — the power stroke — pulling the actin filament past the myosin, and ADP is released.
• A new ATP molecule binds to the myosin head, causing it to detach. ATP hydrolase (activated by Ca²⁺) hydrolyses it, and the energy released recocks the head, ready to bind further along. The cycle repeats while Ca²⁺ and ATP are present.
• On relaxation, Ca²⁺ is actively pumped back into the sarcoplasmic reticulum and tropomyosin re-blocks the binding sites.

The sarcomere on contraction: the I band and the H zone get shorter, and the Z lines move closer together, but the A band stays the same length — because the filaments slide, they do not shorten. This single observation is what proved the theory.

Slow vs fast twitch: slow-twitch fibres contract slowly for a long time, are adapted for aerobic respiration (many mitochondria and capillaries, rich in myoglobin, dark red) — endurance. Fast-twitch fibres contract rapidly and powerfully, are adapted for anaerobic respiration (much glycogen, phosphocreatine store, few mitochondria) and fatigue quickly — sprinting.

Reading a sarcomere

Negative feedback and blood glucose control

Homeostasis is the maintenance of a stable internal environment within narrow limits, which matters because enzymes are sensitive to temperature and pH, and because cells are damaged by osmotic extremes. It works by negative feedback: a deviation is detected by receptors and triggers a response that reverses it. Separate mechanisms for departures in each direction give far more precise control.

Blood glucose is monitored by the islets of Langerhans in the pancreas:

• Too high → β cells secrete insulin → it binds receptors on liver and muscle cells → more glucose transporter (GLUT4) proteins are inserted into the cell-surface membrane, and enzymes are activated for glycogenesis (glucose → glycogen). Glucose uptake and respiration increase, so blood glucose falls.
• Too low → α cells secrete glucagon → liver cells carry out glycogenolysis (glycogen → glucose) and gluconeogenesis (glucose made from glycerol and amino acids). Blood glucose rises.
• Adrenaline also raises blood glucose, by activating glycogenolysis and inhibiting glycogenesis — preparing the body for fight or flight.

The second messenger model: adrenaline (or glucagon) binds to a receptor on the cell surface. This activates adenylate cyclase, which converts ATP into cyclic AMP (cAMP) — the second messenger. cAMP activates protein kinase enzymes, which catalyse the breakdown of glycogen. The hormone itself never enters the cell.

Diabetes: Type I — the β cells are destroyed (autoimmune), so no insulin is produced; treated with insulin injections. Type II — the receptors lose responsiveness to insulin; usually managed by diet, exercise and weight loss, sometimes with drugs.

Your turn — how much glucose?

The nephron and ADH

The kidney filters the blood and controls the water potential of the body fluids.

• Ultrafiltration (Bowman’s capsule): blood in the glomerulus is under high hydrostatic pressure because the afferent arteriole is wider than the efferent arteriole. Water, glucose, ions and urea are forced through the basement membrane (the real filter); blood cells and plasma proteins are too large and stay behind.
• Selective reabsorption (proximal convoluted tubule): all the glucose and most ions are reabsorbed by active transport and co-transport with Na⁺. The epithelial cells have microvilli (huge surface area) and many mitochondria (ATP for active transport). Water follows by osmosis.
• Loop of Henlé — a counter-current multiplier: Na⁺ and Cl⁻ are actively pumped out of the ascending limb, which lowers the water potential of the surrounding medulla. Water therefore leaves the descending limb (which is permeable to water but not ions) by osmosis. The counter-current arrangement means the medulla stays hypertonic all the way down, so water can be drawn out of the collecting duct along its whole length. A longer loop of Henlé → a more concentrated urine — which is why desert mammals have very long loops.
• ADH: osmoreceptors in the hypothalamus detect a fall in the water potential of the blood. The posterior pituitary releases ADH, which makes the collecting duct walls more permeable to water by inserting aquaporins into the membrane. More water is reabsorbed → a small volume of concentrated urine. Drinking a lot of water raises water potential → less ADH → few aquaporins → a large volume of dilute urine.

The counter-current multiplier

Sort the stages of the action potential

Tap a statement, then tap the phase it belongs to.

Structure and function

Tap an item on the left, then its partner on the right.

The big ideas to take away

That is the whole of AQA 3.6 Organisms respond to changes in their internal and external environments. Press Finish to see your score.